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GlyR α3: An Essential Target for Spinal PGE2-Mediated Inflammatory Pain Sensitization
Journal article   Peer reviewed

GlyR α3: An Essential Target for Spinal PGE2-Mediated Inflammatory Pain Sensitization

Robert J Harvey, U B Depner, H Wässle, S Ahmadi, C Heindl, H Reinold, T G Smart, K Harvey, B Schütz, O M Abo-Salem, …
Science, Vol.304(5672), pp.884-887
2004
url
https://doi.org/10.1126/science.1094925View
Published Version

Abstract

biochemistry drug therapy neurology pain sensitization phosphorylation
Prostaglandin E2 (PGE2) is a crucial, mediator of inflammatory pain sensitization. Here, we demonstrate that inhibition of a specific glycine receptor subtype (GlyR α3) by PGE2-induced receptor phosphorylation underlies central inflammatory pain sensitization. We show that GlyR α3 is distinctly expressed in superficial layers of the spinal cord dorsal horn. Mice deficient in GlyR α3 not only lack the inhibition of glycinergic neurotransmission by PGE2 seen in wild-type mice but also show a reduction in pain sensitization induced by spinal, PGE2 injection or peripheral, inflammation. Thus, GlyR α3 may provide a previously unrecognized molecular target in pain therapy.

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